Activation of the autophagy pathway by Torovirus infection is irrelevant for virus replication
Identifieur interne : 000B13 ( Main/Merge ); précédent : 000B12; suivant : 000B14Activation of the autophagy pathway by Torovirus infection is irrelevant for virus replication
Auteurs : Ginés Ávila-Pérez [Espagne] ; Elisabet Diaz-Beneitez [Espagne] ; Liliana L. Cubas-Gaona [Espagne] ; Gliselle Nieves-Molina [Espagne] ; Juan Ram N Rodríguez [Espagne] ; José F. Rodríguez [Espagne] ; Dolores Rodríguez [Espagne]Source :
- PLoS ONE [ 1932-6203 ] ; 2019.
Abstract
Autophagy is a conserved eukaryotic process that mediates lysosomal degradation of cytoplasmic macromolecules and damaged organelles, also exerting an important role in the elimination of intracellular pathogens. Despite the antiviral role of autophagy, many studies suggest that some positive-stranded RNA viruses exploit this pathway to facilitate their own replication. In this study, we demonstrate that the equine torovirus Berne virus (BEV), the prototype member of the
Url:
DOI: 10.1371/journal.pone.0219428
PubMed: 31306441
PubMed Central: 6629058
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PMC:6629058Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Autophagy is a conserved eukaryotic process that mediates lysosomal degradation of cytoplasmic macromolecules and damaged organelles, also exerting an important role in the elimination of intracellular pathogens. Despite the antiviral role of autophagy, many studies suggest that some positive-stranded RNA viruses exploit this pathway to facilitate their own replication. In this study, we demonstrate that the equine torovirus Berne virus (BEV), the prototype member of the <italic>Torovirus</italic>
genus (<italic>Coronaviridae</italic>
Family, <italic>Nidovirales</italic>
Order), induces autophagy at late times post-infection. Conversion of microtubule associated protein 1B light chain 3 (LC3) from cytosolic (LC3 I) to the membrane associated form (LC3 II), a canonical marker of autophagosome formation, is enhanced in BEV infected cells. However, neither autophagy induction, via starvation, nor pharmacological blockade significantly affect BEV replication. Similarly, BEV infection is not altered in autophagy deficient cells lacking either Beclin 1 or LC3B protein expression. Unexpectedly, the cargo receptor p62, a selective autophagy receptor, aggregates within the region where the BEV main protease (M<sup>pro</sup>
) localizes. This finding, coupled with observation that BEV replication also induces ER stress at the time when selective autophagy is taking place, suggests that the autophagy pathway is activated in response to the hefty accumulation of virus-encoded polypeptides during the late phase of BEV infection.</p>
</div>
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